How should presyncope and syncope be managed in heart failure?

Yncope is a sudden and brief loss of consciousness associated with loss of postural tone, from which recovery is spontaneous,’ while presyncope is syncope without the loss of consciousness. They each result from a reduction or brief cessation in cerebral blood flow, and heart disease is a major cause (Table). Syncope and presyncope are the most important predictors of cardiac sudden death, in particular from ventricular arrhythmia. As such, they warrant thorough investigation and careful management, for which a practical framework is given below.

Neurally-mediated reflex syncopal syndromes Crowded environment Volume depletion Cough

Orthostatic hypotension Drug-induced autonomic failure; postural or volume effects on blood pressure (standing still, volume depletion etc) Sinus node dysfunction including bradycardia-tachycardia syndrome

Cardiac arrhythmias Atrioventricular conduction disturbance (2nd- and 3rd-degree atrioventricular block, bundle branch block) Paroxysmal supraventricular and ventricular tachycardia

Noninvasive investigations

These are of limited use in the risk stratification of the individual patient.

ECG monitoring may provide a diagnosis and useful data for arrhythmic risk stratification. It is diagnostic if it provides a correlation between presynco-pal and syncopal symptoms, and reveals bradycardia or tachycardia. Ventricular pauses >3 seconds, phases of second- or third-degree atrioventricular block, and rapid paroxysmal ventricular tachycardia are typical findings.

Echocardiography grades the severity of structural heart disease and its progression over time. Severe aortic stenosis is a structural cause of syncope.

Exercise testing is indicated in syncope occurring during or shortly after exertion. The pathophysiologic basis seems to be exaggerated reflex vasodilatation. The test is diagnostic if it reproduces the hemodynamic abnormalities associated with syncope. A typical finding is Mobitz II second- or third- degree atrioventricular block.

Carotid sinus massage consists of compressing the carotid artery while monitoring the ECG and blood pressure, and is indicated in syncope of unknown etiology. A positive test is asystole >3 seconds and a fall in blood pressure >50 mm Hg.

Tilt testing confirms neurally mediated syncope after other cardiac causes such as arrhythmia have been excluded.

Invasive investigations

Electrophysiologic testing (EPS)

EPS is indicated if the history, ECG, and/or structural heart disease suggest arrhythmia. It is diagnostic if it reveals any of the following: sinus bradycardia and a very long sinus node recovery time; baseline HV interval >100 ms (debatable); second- and third-degree block induced during incremental atrial pacing; or induced mono/polymorphous ventricular tachyarrhythmias or rapid symptomatic supraventricular arrhythmias.

The sensitivity, specificity, and predictive value of EPS depend on the clinical presentation and underlying structural disease. The induction of sustained ventricular arrhythmia by EPS identifies high-risk coronary patients with syncope. Recent evidence from clinical trials such as the Multicenter Autonomic Defibrillator Implantation Trial II (MADIT II) also suggests that a depressed left ventricular ejection fraction in ischemic cardiomyopathy without criteria for arrhythmia is an independent predictor of arrhythmic sudden death. On the other hand, in patients with nonischemic cardiomyopathy, heart failure, and unexplained syncope, the negative predictive value is low and noninducibility does not signify a low risk of arrhythmic death.

Cardiac catheterization and angiography

If noninvasive assessment suggests acute myocardial ischemia as the trigger to syncope, by triggering ventricular tachycardia or drastically decreasing cardiac output during ischemia, then coronary angiography is required to assess the severity of coronary heart disease with a view to revascularization.

Therapy

In conditions for which an arrhythmic cause has been excluded, such as neurally mediated reflex syncope and orthostatic hypotension, treatment aims to prevent recurrence and improve quality of life. It is usually sufficient to explain the benign nature of the condition, and give advice on avoiding trigger agents, in particular relating to antihypertensive therapy.

In arrhythmic syncope, treatment is also designed to prevent recurrence and improve quality of life, but in addition to decrease mortality. A pacemaker should be considered for sinus node dysfunction or an atrioventricular conduction disturbance. The treatment of choice for paroxysmal supraventricular arrhythmia causing syncope is transcatheter ablation. Syncope caused by ventricular tachycardia in heart failure is usually treated with an autonomic implantable cardioverter-defibrillator (AICD), although in a few specific forms, namely right ventricular outflow tract tachycardia and bundle branch reentry tachycardia, ablation is the appropriate first-line therapy.

The American College of Cardiology/American Heart

Association have issued the following guidelines on the indications for AICD therapy:

Class I. Syncope of undetermined origin with clinically relevant, hemodynamically significant EPS-induced ventricular tachycardia or fibrillation, when drug therapy is ineffective, poorly tolerated, or not preferred.

Class lib. Recurrent syncope of undetermined etiology in the presence of ventricular dysfunction and EPS-inducible ventricular arrhythmia after excluding other causes.

MADIT II was stopped early because it showed that mortality was 30% lower in the patients treated by implantable defibrillator vs those receiving antiarrhythmic medication. Since these patients had no criteria for arrhythmia, it is reasonable to assume that future indications for prophylactic AICD will extend beyond malignant arrhythmia, a frequent cause of syncope in heart failure, to include all cases of ischemic heart failure with a history of syncope but no documented arrhythmia.

Further reading

Brignoie M, Alboni P, BendHt D, et al. Task Force on Syncope, European Society of Cardiology. Part 2. Diagnostic tests and treatment: summary of recommendations. Europace. 2001;3:261-268.

Coats AJ. MADIT II, the Multi-center Autonomic Defibrillator Implantation Trial II stopped early for mortality reduction, has ICD therapy earned its evidence-based credentials? IntJ Cardiol. 2002;82:1-5.

Gregoratos G, Cheitfin MD, Conill A, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). Circulation. 1998;97:1325-1335.

Kapoor WN. Syncope. N Engl J Med. 2000;343:1856-1862.

Kapoor WN, Hanusa BH. Is syncope a risk factor for poor outcomes? Comparison of patients with and without syncope. Am J Med. 1996; 100:646-655. Saeed M, Homoud MK, Wang PJ, Estes NA, Link MS. Rote of invasive electrophysiologic testing in risk stratification for sudden cardiac death. J Invasive Cardiol. 2001 ;13:758-762.

Keywords

symptom; diagnosis; syncope; presyncope; therapy

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